Hemorheology in the erythrocytoses

In vitro, rheological studies establish that whole blood viscosity and yiel d stress are high in patients with an erythrocytosis. However a number of f actors ensure that these patients, under physiological conditions, do not s how the clinical features observed in other hyperviscosity states. These in clude red cell axial migration in flowing blood and "plug flow" in the larg est vessels. In addition, a small increase in vessel diameter leads to larg e increases in blood flow, and generally high blood flows produce the lowes t blood viscosity values. The increased hemoglobin levels and the increase in oxygen-carrying capacity at high hematocrit values compensate for the ti ssue hypoxia. In the "non-hypoxemic" erythrocytosis (polycythemia vera, idi opathic and apparent erythrocytosis), there is an increased incidence of va scular occlusion in untreated patients. The reasons for this include reduce d peripheral blood flow, increased platelet-vessel wall interactions, and t he demonstrated in vitro hyperviscosity which comes into Flay with abnormal ly low flow, seen in vivo under pathological conditions. In the erythrocyto sis of hypoxemic lung disease and its associated hypoxemia, pulmonary vasoc onstriction enhances susceptibility to hyperviscosity effects in particular . Moreover, the vasoconstriction caused by the hypoxemia prevents the norma l adaptive changes of increased vessel diameter. Microcytic hypochromic red cell changes of iron deficiency do not cause a higher viscosity value at a ny given hematocrit value compared with normal red cells. However, in hypox emic states oxygen-carrying capacity should he maximized, since the hemoglo bin value is disproportionately lower at any given hematocrit in the presen ce of microcytic hypochromic cells compared with normal red cells.